Air Care / Annals of B Pod Series: Hypokalemia
/History of Present Illness
Air Care was dispatched to a referring hospital for a middle aged male who presented with lower extremity weakness. Upon presentation to the hospital, the patient was somnolent with weakness in the bilateral lower extremities and full strength in his upper extremities. Providers were concerned for stroke. The patient underwent a non-contrast CT scan and prior to any therapeutic interventions suffered a pulseless electrical activity (PEA) arrest. The patient received chest compressions and two rounds of epinephrine with return of spontaneous circulation (ROSC) before a second pulse check. The patient was intubated and started on an amiodarone drip following a brief episode of wide complex tachycardia. Following ROSC the patient’s labs resulted with a potassium of 1.5 mEq/L.10 mEq of potassium chloride was started via a peripheral line.
Past Medical History
Bipolar disorder, morbid obesity, hypertension, hyperlipidemia, COPD
Past Surgical History Unknown
Family History Unknown
Medications Unknown
Allergies Unknown
Vitals
HR: 88, BP: 90/60, RR: 24, SpO2: 84% (on 100% FiO2, PEEP 8)
Ventilator setting
Assist Control - Tidal Volume 550cc, RR 16, FiO2 100%, PEEP 8
Physical Exam
The patient was pale, obese, and ill appearing on the ventilator. Breath sounds were symmetric. Patient was in normal sinus rhythm on the monitor, with occasional premature ventricular complexes (PVCs). The patient’s pupils were equal, round and reactive to light (4-->2mm). He opened his eyes and moved all four extremities to command.
Pre-Hospital Interventions
Upon HEMS arrival, the first 10 mEq of potassium had completed administration. An additional 10 mEq of potassium was ordered and administered prior to departure. Immediately after takeoff, the patient became bradycardic to the 20s and pulseless. The patient underwent resuscitation via ACLS guidelines, and ROSC was achieved after 8 minutes.
The patient remained hypotensive with a normal sinus rhythm and frequent PVCs. The remaining potassium was rapidly administered intravenous push with resolution of the patient’s PVCs. 20 ug of epinephrine was administered with improvement in blood pressure to 100/60. The patient remained stable throughout the rest of the flight. At the receiving tertiary care center the patient’s initial blood gas was significant for a normal pH and potassium of 1.7 mEq/L.
Discussion
Potassium was first isolated from potash by Sir Humphrey Davy in 1807, but the biologic significance of potassium was not recognized until over one hundred years later. Potassium is primarily an intracellular cation, with concentrations 30- 40-fold greater intracellularly than extracellularly. This differential is achieved by the sodium-potassium ATPase enzyme found in the plasma membrane of cells. ATPase hydrolyzes ATP to pump three sodium ions out of the cell in exchange for two extracellular potassium ions into the cell. This gradient facilitates an outward current of potassium through potassium-selective ion channels in the plasma membrane resulting in a negative resting membrane potential (RMP) in the cardiac myocyte. The negative RMP works to stabilize excitable tissue, such as atrial and ventricular myocytes, thus preventing spontaneous action potentials. With hypokalemia, the repolarization reserve is reduced. This leads to intracellular sodium and calcium accumulation leading to early after-depolarization arrhythmias such as polymorphic ventricular tachycardia (VT), which can degenerate to ventricular fibrillation (VF) causing sudden cardiac death.
Hypokalemia is defined as potassium less than 3.6 mEq/L (3.6 mmol/L) and is present in up to 21% of hospitalized patients and 2-3% of outpatients. (1-3) The most frequent causes of hypokalemia are diuretic use and gastrointestinal (GI) illness. Diuretic-induced hypokalemia occurs through direct renal loss, is dose-dependent, and tends to be mild (3 - 3.5 mEq/L). (4) The mechanism by which upper GI loss induces hypokalemia is indirect and is thought to result from a maladaptive renal response to the vomiting induced alkalosis. Lower GI losses in the form of diarrhea can also result in hypokalemia, as a portion of daily potassium is excreted in the colon. Hypokalemia secondary to lower GI losses may be accompanied by hyperchloremic acidosis. (5) Less common causes of hypokalemia include renal tubular acidosis, transcellular shift, and inadequate intake.
It is important to evaluate for possible GI losses, review medications (diuretics, laxatives etc.), and assess for underlying cardiac comorbidities. Neurologic manifestations can range from generalized weakness to ascending paralysis, though the latter is uncommonly seen. Early cardiac effects of hypokalemia can be demonstrated on EKG. Initial changes include T wave flattening/inversion, PR prolongation, prominent U waves, and ST depression as shown in Figure 1. The U wave is a small (0.5 mm) deflection immediately following and in the same direction as the T wave, best seen in V2 and V3. (6) The later cardiac effects of hypokalemia include fatal arrhythmias such as bradycardia, ventricular tachycardia, ventricular fibrillation, and Torsades de Pointes. “Classic” ECG findings have poor sensitivity for diagnosing hypokalemia, as many patients with low potassium have a normal ECG.
Prior to initiation of treatment for hypokalemia it is first important to assess whether the patient has pseudohypokalemia. Pseudohypokalemia is an aberrant laboratory phenomena where a sample from a patient with a normal potassium is reported as hypokalemic. This is a laboratory phenomenon caused by both delayed sample analysis and leukocytosis. When rechecked the potassium will usually be normal provided sample analysis is not again delayed. It is however important not to delay potassium administration in a patient with a classic history and EKG changes while awaiting confirmation. Once the diagnosis of hypokalemia is certain further laboratory work-up must be pursued if a cause is not known. When there is concern for renal losses of potassium, urine potassium and potassium-to-creatinine ratios should be checked.
Initial treatment is focused on preventing cardiac conduction disturbances and neuromuscular dysfunction by repleting potassium. Goal potassium levels are > 3.6 mEq/L for the general population and > 4.0 mEq/L for patients with a history of heart failure or myocardial infarction (6) Empiric administration of magnesium should be considered as patients will be unable to absorb potassium in a hypomagnesemic state. This is a consequence of the effects of magnesium on the luminal potassium (ROMK) channels within the connecting tubule and cortical collecting tubules of the kidney. Low levels of intracellular magnesium decrease the magnesium-mediated inhibition of the ROMK channels leading to increased renal potassium secretions, ultimately decreasing the efficacy of potassium replacement. (7)
Replacement of potassium is simple and formulaic. Serum potassium concentration decreases approximately 0.3 mEq/L (0.3 mmol/L) for every 100 mEq (100 mmol) reduction in total body potassium. (8) Using the patient’s measured potassium level, this can be used to estimate the amount of potassium needed (Table 3) to correct the patient’s hypokalemia. Oral potassium is the preferred route of administration with intravenous potassium reserved for patients with ECG changes, physical signs or symptoms of hypokalemia, inability to tolerate potassium by mouth or severe hypokalemia (<2.5 mEq/L). Intravenous potassium correction should not exceed 20 mEq/hour except for emergent situations and where central venous access is available. (9) Administration of potassium at rates exceeding 20 mEq/hour may cause cardiac toxicity, including arrhythmias and cardiac arrest. Patients should be monitored on a continuous cardiac monitor and the serum potassium level should be measured hourly when intravenous potassium is administered at rates exceeding 20 mEq/hour. Additionally, infusion site checks should be conducted regularly as high concentrations administered via a peripheral line can cause phlebitis and pain. (10) Identification and treatment of concurrent hypomagnesemia are also important because magnesium depletion impedes potassium repletion and can exacerbate hypokalemia-induced rhythm disturbances. (11, 12) Dextrose containing solutions can worsen hypokalemia and should not be used as the replacement fluid. All patients should have cardiac monitoring while potassium is being replaced intravenously.
While hyperkalemia is the more commonly encountered and feared complication of abnormal potassium homeostasis, hypokalemia too can be devastating. When concerned for hypokalemia always assess the cardiac and neurologic status, confirm the diagnosis with repeat labs if time/acuity permits, and initiate treatment early once the diagnosis is made. Oral and intravenous potassium are the initial treatment. Simultaneous magnesium administration should be considered particularly if magnesium levels are unknown. All patients should have EKGs performed to assess for cardiac abnormalities. Initial efforts should be focused on replacement and resuscitation but exploring the potential etiology of the patients hypokalemia can serve to guide inpatient management.
AUTHORED BY ADAM GOTTULA, MD
Dr. Gottula is a third-year Emergency Medicine resident at the University of Cincinnati
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